Visar resultat 1 - 5 av 9 avhandlingar innehållade ordet ADRA2A.
Sammanfattning : Defective insulin secretion is a central feature in diabetes mellitus and results from reduced pancreatic beta-cell mass as well as aberrant beta-cell function. The pathophysiology of diabetes is incompletely known, but a strong hereditary component is suggested. LÄS MER
Sammanfattning : Defective insulin secretion from the pancreatic B-cells is a central feature in type 2 diabetes (T2D). There is a strong hereditary component in type T2D, but the underlying pathophysiology remains largely unknown. LÄS MER
Sammanfattning : Type 2 diabetes is caused by a combination of environmental and inherited factors influencing the progression of insulin resistance and impaired insulin secretion leading to chronically elevated blood glucose levels. The aim of this thesis was to functionally and genetically characterise the species-conserved diabetes locus Niddm1i of the GK rat encoding hyperglycaemia and defect insulin secretion. LÄS MER
4. Identification of new disease mechanisms and treatments for type 2 diabetes based on genetic variants and gene expression networks
Sammanfattning : Improved understanding of the disease mechanisms underlying type 2 diabetes (T2D) is needed, and so are new treatments.A new T2D risk variant was recently identified in ADRA2A, which encodes the α2A-adrenergic receptor. LÄS MER
Sammanfattning : Type 2 diabetes (T2D) is a polygenic disease caused by an interaction between genetic and environmental factors such as low physical activity, smoking, and obesity. The disease is associated with devastating chronic microvascular (nephropathy, retinopathy, and neuropathy) and macrovascular (coronary heart disease and stroke) complications. LÄS MER